Difference between revisions of "Polyneuritis Equi"

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 +
* A non-infectious [[CNS Inflammation - Pathology|central nervous inflammatory disease]]
 +
* Polyneuritis equi (PNE) is an uncommon disease which affects mature horses
 +
* Formerly known as 'cauda equina syndrome' or 'cauda equina neuritis'
 +
* May occur as:
 +
** A disease effecting the spinal nerve roots and ganglia of the cauda equina.
 +
** A disease effecting the cranial nerves.
 +
* 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.
 +
* If the pelvic nerve roots are also involved, there may be changes in hindlimb gait.
 +
* Cranial nerve signs may be apparent, including signs associated with facial nerve paralysis.
 +
* Changes in the CSF are often non-specific.
 +
** There is usually a moderate mononucloear pleocytosis.
 +
** Protein is usually elveated.
 +
* Histologically, the disease presents as a severe, chronic, destructive lymphocytic and histiocytic polyradiculoneuritis.
 +
* 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
 +
* Disease appears similar to:
 +
** Guillain-Barré Syndrome (GBS), an autoimmune demyelinating diease in humans
 +
** Experimental allergic neuritis (EAN) in laboratory animals
 +
* Important differential diagnoses for progressive neurologic signs effecting the bladder, rectum, perineum, tail, penis and hindlimbs in horses include:
 +
** Equine herpesvirus-1 myeloencephalopathy
 +
** Sacral/coccygeal trauma
 +
** Equine motor neuron disease
 +
** Abberant parasite migration (e.g. ''Strongylus spp.'')
 +
** In endemic areas, ''Sarcocystis neurona'' myelitis (equine protozoal myelitis), rabies and ''rhodococcus equi'' myeloencepahlitis should also be considered.
  
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|Equine Herpesvirus-1]] and ''[[Campylobacter species - Overview|Campylobacter]]'' have been proposed, but there has been no confirmation.
+
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
  
It is seen in '''adult horses of all breeds in North America and Europe'''.
+
Cauda Equina Neuritis - large animals
 +
:Equine version of Idiopathic polyradiculoneuritis
 +
:Extradural nerve roots of cauda equina thickened and discoloured
 +
:Inflammatory infiltrate (lymphocytes, plasma cells, macrophages)
 +
:Extensive axonal damage and demyelination
 +
:Cranial nerve involvement often occurs
 +
:Aetiology unknown:
 +
:Antecedent infection?
 +
:Antibodies to PNS myelin?
 +
:Paralysis & anaesthesia of tail
 +
:Urinary incontinence
 +
:Loss of anal reflex
 +
:Failure to defaecate
 +
:Pain/hypersensitivity in gluteal/tail-head area
 +
:Clinical signs
 +
:Recovery unlikely - most animals are destroyed.
  
==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 Nerves - Anatomy & Physiology|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 testing|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 [[Cerebral Spinal Fluid - Anatomy & Physiology|'''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|Equine herpesvirus-1]] myeloencephalopathy
 
:Sacral/coccygeal trauma
 
:[[Equine Motor Neuron Disease|Equine motor neuron disease]]
 
: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]])
 
:[[Rabies]] and ''[[Rhodococcus equi]]'' myeloencephalitis 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''
 
 
{{review}}
 
 
==Webinars==
 
<rss max="10" highlight="none">https://www.thewebinarvet.com/neurology/webinars/feed</rss>
 
 
[[Category:Neurological Diseases - Horse]]
 
[[Category:Expert Review - Horse]]
 
 
[[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 14:19, 9 March 2011

  • A non-infectious central nervous inflammatory disease
  • Polyneuritis equi (PNE) is an uncommon disease which affects mature horses
  • Formerly known as 'cauda equina syndrome' or 'cauda equina neuritis'
  • May occur as:
    • A disease effecting the spinal nerve roots and ganglia of the cauda equina.
    • A disease effecting the cranial nerves.
  • 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.
  • If the pelvic nerve roots are also involved, there may be changes in hindlimb gait.
  • Cranial nerve signs may be apparent, including signs associated with facial nerve paralysis.
  • Changes in the CSF are often non-specific.
    • There is usually a moderate mononucloear pleocytosis.
    • Protein is usually elveated.
  • Histologically, the disease presents as a severe, chronic, destructive lymphocytic and histiocytic polyradiculoneuritis.
  • 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
  • Disease appears similar to:
    • Guillain-Barré Syndrome (GBS), an autoimmune demyelinating diease in humans
    • Experimental allergic neuritis (EAN) in laboratory animals
  • Important differential diagnoses for progressive neurologic signs effecting the bladder, rectum, perineum, tail, penis and hindlimbs in horses include:
    • Equine herpesvirus-1 myeloencephalopathy
    • Sacral/coccygeal trauma
    • Equine motor neuron disease
    • Abberant parasite migration (e.g. Strongylus spp.)
    • In endemic areas, Sarcocystis neurona myelitis (equine protozoal myelitis), rabies and rhodococcus equi myeloencepahlitis should also be considered.


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

Cauda Equina Neuritis - large animals

Equine version of Idiopathic polyradiculoneuritis
Extradural nerve roots of cauda equina thickened and discoloured
Inflammatory infiltrate (lymphocytes, plasma cells, macrophages)
Extensive axonal damage and demyelination
Cranial nerve involvement often occurs
Aetiology unknown:
Antecedent infection?
Antibodies to PNS myelin?
Paralysis & anaesthesia of tail
Urinary incontinence
Loss of anal reflex
Failure to defaecate
Pain/hypersensitivity in gluteal/tail-head area
Clinical signs
Recovery unlikely - most animals are destroyed.