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{| cellpadding="10" cellspacing="0" border="1"
 
{| cellpadding="10" cellspacing="0" border="1"
 
| Also known as:
 
| Also known as:
| '''Autonomic Polygangioneuropathy'''<br>
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| '''Autonomic Polyganglioneuropathy'''<br>
 
'''Feline Dysautonomia'''
 
'''Feline Dysautonomia'''
 
|}
 
|}
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===Pharmalogical Tests===
 
===Pharmalogical Tests===
* Topical ocular administration of dilute pilocarpine - miosis implies a postive result. However, not all respond. Response is dependent on damage to the postganglionic parasympathetic neuron causing supersensitivity of the iris muscle
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Various provocative tests can be used to assess the autonomic nerbous systems of animals with suspected Key-Gaskell syndrome:
* IV or SC administration of atropine (a parasympatholytic) - lack of increase in heart rate implies a positive result
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*Topical ocular administration of dilute pilocarpine should result in miosis, which implies a postive result. However, not all animals respond and the response is dependent on the degree of damage to the postganglionic parasympathetic neuron causing (denervation) supersensitivity of the iris muscle.
* ID administration of histamine - the wheal and flare response may be dampened in those with dysautonomia
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*Intra-venous or subcutaneous administration of atropine (a parasympatholytic) should result in an increase in the heart rate.  A failure to respond implies a positive result.
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*Intra-dermal administration of histamine should result in a classical wheal and flare response but this may be dampened in those animals with dysautonomia.  An absence of the wheal and flare response is therefore a positive result.
    
=====Pathology=====
 
=====Pathology=====
 
[[Image:Ba 250 07.jpg|thumb|Histological section of a degenerate neuron from a cat with Key-Gaskell Syndrome<br><small>Copyright Susan Rhind 2007 RVC]]</small>  
 
[[Image:Ba 250 07.jpg|thumb|Histological section of a degenerate neuron from a cat with Key-Gaskell Syndrome<br><small>Copyright Susan Rhind 2007 RVC]]</small>  
*Histologically there is marked reduction in the number of neurones in all autonomic ganglia in the ventral horn of all levels of spinal cord accompanied by proliferation of non-neuronal cells.
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*Histologically there is marked reduction in the number of neurones in all autonomic ganglia in the ventral horn of all levels of spinal cord accompanied by proliferation of non-neuronal cells. Similar changes are found in the brainstem nuclei of the cranial nerves and features of chromatolytic degeneration may be apparent in the ganglia, spinal cord and sympathetic axons.
*Similar changes in brain stem nuclei of cranial nerves.
  −
===Histological Findings===
  −
Chromatolytic degeneration in autonomic ganglia, spinal cord intermediate grey columns and some sympathetic axons.
      
==Differential Diagnosis==
 
==Differential Diagnosis==
There are few differentials on presentation of the many manifestations of the disease. However, early in the course of disease other causes of megaoesophagus need to be considered.
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There are few differential diagnoses for this clinical presentation but, early in the course of disease, other causes of [[Megaoesophagus|megaoesophagus]] should be considered.
 
      
==Treatment==
 
==Treatment==
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===Parasympathomimetic Drugs===
 
===Parasympathomimetic Drugs===
 
Some dogs may show minor improvement on initiation of for example, bethanechol, metoclopramide.
 
Some dogs may show minor improvement on initiation of for example, bethanechol, metoclopramide.
      
==Prognosis==
 
==Prognosis==
 
Guarded to poor. Recovery rates in the cat are reported as 20-40%, however this may take 2-12 months. In the dog recovery rates are lower. Despite recovery many are also left with residual impairment including intermittent regurgitation.
 
Guarded to poor. Recovery rates in the cat are reported as 20-40%, however this may take 2-12 months. In the dog recovery rates are lower. Despite recovery many are also left with residual impairment including intermittent regurgitation.
      
==References==
 
==References==
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