Difference between revisions of "Polyneuritis Equi"

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* A non-infectious [[CNS Inflammation - Pathology|central nervous inflammatory disease]]
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Also know as: '''''Neuritis of the cauda equina — Cauda equina syndrome — Cauda equina neuritis'''''
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* Polyneuritis equi (PNE) is an uncommon disease which affects mature horses
 
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* Formerly known as 'cauda equina syndrome' or 'cauda equina neuritis'
 
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* May occur as:
 
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** A disease effecting the spinal nerve roots and ganglia of the cauda equina.
 
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** A disease effecting the cranial nerves.
 
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* Cauda equina disease is characterised by progressive loss of anal tone, tail paralysis, urinary and/or faecal incontinence, urine scalding of the hindlimbs, hyperaesthesia and muscle fasciculations over hindquarters.
 
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* If the pelvic nerve roots are also involved, there may be changes in hindlimb gait.
 
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* Cranial nerve signs may be apparent, including signs associated with facial nerve paralysis.
 
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* Changes in the CSF are often non-specific.
 
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** There is usually a moderate mononucloear pleocytosis.
 
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** Protein is usually elveated.
 
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* Histologically, the disease presents as a severe, chronic, destructive lymphocytic and histiocytic polyradiculoneuritis.
 
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* Pathogenesis is not completely understood, but considered to be a T-lymphocyte mediated response to myelin, followed by destruction of myelin and axons by macrophages
 
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* Disease appears similar to:
 
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** Guillain-Barré Syndrome (GBS), an autoimmune demyelinating diease in humans
 
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** Experimental allergic neuritis (EAN) in laboratory animals
 
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* Important differential diagnoses for progressive neurologic signs effecting the bladder, rectum, perineum, tail, penis and hindlimbs in horses include:
 
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** Equine herpesvirus-1 myeloencephalopathy
 
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** Sacral/coccygeal trauma
 
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** Equine motor neuron disease
 
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** Abberant parasite migration (e.g. ''Strongylus spp.'')
 
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** In endemic areas, ''Sarcocystis neurona'' myelitis (equine protozoal myelitis), rabies and ''rhodococcus equi'' myeloencepahlitis should also be considered.
 
  
 +
==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 American 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 variable 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'''.
 +
 +
{{Learning
 +
|flashcards = [[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''
 +
 +
[[Category:To Do - Helen]]
 +
[[Category:To Do - Review]]
  
  
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:Persist for >3 months if possible
 
:Persist for >3 months if possible
  
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Cauda Equina Neuritis - large animals
 
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:Equine version of Idiopathic polyradiculoneuritis
 
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:Extradural nerve roots of cauda equina thickened and discoloured
 
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:Inflammatory infiltrate (lymphocytes, plasma cells, macrophages)
 
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:Extensive axonal damage and demyelination
 
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:Cranial nerve involvement often occurs
 
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:Aetiology unknown:
 
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:Antecedent infection?
 
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:Antibodies to PNS myelin?
 
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:Paralysis & anaesthesia of tail
 
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:Urinary incontinence
 
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:Loss of anal reflex
 
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:Failure to defaecate
 
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:Pain/hypersensitivity in gluteal/tail-head area
 
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:Clinical signs
 
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:Recovery unlikely - most animals are destroyed.
 
  
 
[[Category:Central Nervous System - Idiopathic Pathology]]
 
[[Category:Central Nervous System - Idiopathic Pathology]]
 
[[Category:Peripheral Nervous System - Pathology]]
 
[[Category:Peripheral Nervous System - Pathology]]

Revision as of 08:28, 4 August 2011

Also know as: Neuritis of the cauda equina — Cauda equina syndrome — Cauda equina neuritis

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 American 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 variable 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
FlashcardsFlashcards logo.png
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


Cauda Equina Traction - in small animals

Tail pull injury
Esp. cats after RTA
Lesion via longitudinal traction
Sacrocaudal dislocation/fracture
Limp tail
Incontinence
Hindlimb Paresis
Diagnosis on Clinical signs and history
+/- Radiographs to show dislocation/fracture
Prognosis difficult to predict
Poor prognosis if tail limp & no anal tone
Supportive treatment
Persist for >3 months if possible
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