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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>
| '''Autonomic Polyganglioneuropathy'''<br>
'''Feline Dysautonomia'''
'''Feline Dysautonomia'''
|}
|}
===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
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
*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
*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.
*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.
*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.
==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.
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==
===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==