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Wednesday, January 09, 2008

Exopthalmus is not a sign of stellate ganglion block

025. Which of the following is not a sign of stellate ganglion block?

1. Meiosis

2. exopthalmus

3. Nasal congestion

4. Conjuctival redness


2. Exopthalmus


Oxford Text book of Surgery, Chapter. 7.9.2

Bailey and Love 24th Edition, Page 953

Concise text book of Surgery, 3rd Edition, Page 154




Repeat. Asked in AIPG 2005


Most books


Damage to the stellate ganglion results in a Horner's syndrome with ptosis, pupillary constriction, and facial flushing and dryness on the affected side. Though cycloplegia does not occur, there may be difficulties in accomodation


Horner's syndrome is characterized by an interruption of the oculosympathetic nerve pathway somewhere between its origin in the hypothalamus and the eye. The classic clinical findings associated with Horner's syndrome are ptosis, pupillary miosis and facial anhidrosis. Other findings may include apparent enophthalmos, increased amplitude of accommodation, heterochromia of the irides (if it occurs before age two), paradoxical contralateral eyelid retraction, transient decrease in intraocular pressure and changes in tear viscosity.


Sympathetic innervation to the eye consists of a three neuron arc. The first neuron originates in the hypothalamus. It descends and travels between the levels of the eighth cervical and forth thoracic vertebrae (C8-T4) of the spinal cord. There, it synapses with second order neurons whose preganglionic cell bodies give rise to axons. These axons pass over the apex of the lung and enter the sympathetic chain in the neck, synapsing in the superior cervical ganglion. Here, cell bodies of third order neurons give rise to postganglionic axons that course to the eye via the cavernous sinus. These sympathetic nerve fibers course anteriorly through the uveal tract and join the fibers of long posterior ciliary nerves to innervate the dilator of the iris. Postganglionic sympathetic fibers also innervate the muscle of Mueller within the eyelid, which is responsible for the initiation of eyelid retraction during eyelid opening. Postganglionic sympathetic fibers, responsible for facial sweating, follow the external carotid artery to the sweat glands of the face. Interruption at any location along this pathway (preganglionic or postganglionic) will induce an ipsilateral Horner's syndrome.

The common etiologies of acquired preganglionic Horner's syndrome include, but are not limited to, trauma, aortic dissection, carotid dissection, tuberculosis and Pancoast tumor. Common causes of post-ganglionic Horner's syndrome include trauma, cluster migraine headache and neck or thyroid surgery.


The diagnosis and the localization of a Horner's syndrome is accomplished with pharmacological testing. Ten percent liquid cocaine (topically applied), works as an indirect acting sympathomimetic agent by inhibiting the re-uptake of norepinephrine at the nerve ending. A Horner's pupil will dilate poorly because of the absence of endogenous norepinephrine at the nerve ending. The test should be evaluated thirty minutes after the instillation of the drops to ensure accuracy. The cocaine test is used to confirm or deny the presence of a Horner's syndrome. However, a positive cocaine test does not localize the lesion.

To localize the lesion as either preganglionic or postganglionic, Paradrine 1% (hydroxyamphetamine) or Pholedrine 5% (n-methyl derivative of hydroxyamphetamine) can be instilled 48 hours later. Pholedrine and Paradrine act similarly by producing the forced release of endogenous norepinephrine from the presynaptic vesicles. If the third neuron is damaged, there will be no endogenous norepinephrine and the pupil will not dilate, thus indicating a postganglionic lesion. Dilation indicates first or second order neuron lesion. There is currently no method of topical testing to differentiate a first order preganglionic lesion from a second order preganglionic lesion.

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