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Bundle of nerves, parasympathetic ganglion From Wikipedia, the free encyclopedia
The ciliary ganglion is a parasympathetic ganglion located just behind the eye in the posterior orbit. It is 1–2 mm in diameter and in humans contains approximately 2,500 neurons.[1] The ganglion contains postganglionic parasympathetic neurons. These neurons supply the pupillary sphincter muscle, which constricts the pupil, and the ciliary muscle which contracts to make the lens more convex. Both of these muscles are involuntary since they are controlled by the parasympathetic division of the autonomic nervous system.
| Ciliary ganglion | |
|---|---|
| |
 Detailed view of nerves of lateral orbit showing the ciliary ganglion immediately behind the globe of the eye. | |
| Details | |
| From | Sensory root of ciliary ganglion
sympathetic root of ciliary ganglion parasympathetic root of ciliary ganglion |
| To | Short ciliary nerves |
| Identifiers | |
| Latin | ganglion ciliare |
| TA98 | A14.3.02.003 |
| TA2 | 6663 |
| FMA | 6964 |
| Anatomical terms of neuroanatomy | |
The ciliary ganglion is one of four parasympathetic ganglia of the head. The others are the submandibular ganglion, pterygopalatine ganglion, and otic ganglion.
The ciliary ganglion contains postganglionic parasympathetic neurons that supply the ciliary muscle and the pupillary sphincter muscle. Because of the much larger size of the ciliary muscle, 95% of the neurons in the ciliary ganglion innervate it compared to the pupillary sphincter.
Three types of axons enter the ciliary ganglion but only the preganglionic parasympathetic axons synapse there. The entering axons are arranged into three roots which join enter the posterior surface of the ganglion:
Exiting from the anterior surface of the ciliary ganglion are the short ciliary nerves which contain the sensory, postganglionic sympathetic and postganglionic parasympathetic axons to the eye.
Diseases of the ciliary ganglion produce a "tonic pupil",[2] which is a pupil that does not react to light (it is “fixed”) and has an abnormally slow and prolonged response to attempted near vision (accommodation).
When a person with an Adie pupil attempts to focus on a nearby object, the pupil (which would normally constrict rapidly) constricts slowly. On close inspection, the constricted pupil is not perfectly round. When the person focuses on a more distant object (say the far side of the room), the pupil (which would normally dilate immediately) remains constricted for several minutes, and then slowly dilates back to the expected size.
Tonic pupils are fairly common – they are seen in roughly 1 out of every 500 people. A person with anisocoria (one pupil bigger than the other) whose pupil does not react to light (does not constrict when exposed to bright light) most likely has Adie syndrome – idiopathic degeneration of the ciliary ganglion.
The strange behavior of tonic pupils was first explained by Irene Loewenfeld in 1979. The ciliary ganglion contain many more nerve fibers directed to the ciliary muscle than nerve fibers directed to the constrictor pupillae – roughly twenty times more. The ciliary muscle is also more massive than the constrictor pupillae, again by a factor of twenty. Based on these observations, Loewenfeld proposed an explanation of the tonic pupil. She noted that pathological destruction of nerve cells in the ciliary ganglion that is found in all cases of Adie pupil. In her own words:[3]
Loewenfeld’s theory is now generally accepted. It explains the defining features of a tonic pupil:
Tonic pupils are usually due to Adie syndrome, but other diseases can denervate the ciliary ganglion. Peripheral neuropathies (such as diabetic neuropathy) occasionally produce tonic pupils. Herpes zoster virus can attack the ciliary ganglion. Trauma to the orbit can damage the short ciliary nerves. Anything that denervates the ciliary ganglion will produce a tonic pupil due to aberrant nerve regeneration.
Adie syndrome[4] is tonic pupil plus absent deep tendon reflexes. Adie syndrome is a fairly common, benign, idiopathic neuropathy that selectively affects the ciliary ganglion and the spinal cord neurons involved in deep tendon reflex arcs. It usually develops in middle age, although it can occur in children. A variant of Adie syndrome, Ross syndrome, affects sweating as well.
Early in the course of Adie syndrome (when the cells of the ciliary ganglion have been destroyed, but before regeneration has occurred) the pupil will be fixed and dilated. The sphincter pupillae will be paralyzed. There will be no response to accommodation – the ciliary muscle is also paralyzed.
With aberrant nerve regeneration, the pupil will remain fixed, but it will constrict with attempted near vision. The constriction will be abnormal (“tonic”).
Late in the course of Adie syndrome, the pupil becomes small (as all pupils do with old age). It will still be “fixed” (it will not constrict to bright light) and it will continue to show abnormal, tonic constriction with attempted near vision.
In some neurological disorders, the pupil does not react to light, but it does react to accommodation. This is called “light-near dissociation”.
In Adie syndrome, damage involving the ciliary ganglion manifests light-near dissociation and a tonically dilated pupil (usually on the same side).
Other causes of light-near dissociation involve damage to the brainstem,[citation needed] where a tonic pupil is not produced. Brainstem causes of light-near dissociation include Argyll Robertson pupil and Parinaud syndrome.
Irene Loewenfeld is generally credited for being the first physiologist to make this distinction.
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