rnous sinus thrombosis
- Nerve blocks, such as cervical plexus block, stellate ganglion or interscalene block
Horner's syndrome is due to a deficiency of sympathetic activity. The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms. The following are examples of conditions that cause the clinical appearance of Horner's syndrome:
- First-order neuron disorder: Central lesions that involve the hypothalamospinal pathway (e.g. transection of the cervical spinal cord).
- Second-order neuron disorder: Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor).
- Third-order neuron disorder: Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus).
Three tests are useful in confirming the presence and severity of Horner's syndrome:
- Cocaine drop test - Cocaine blocks the reuptake of norepinephrine resulting in the dilation of a normal pupil. Due to the lack of norepinephrine in the synaptic cleft, the pupil will fail to dilate in Horner's syndrome.
- Paredrine test:- This test helps to localize the cause of the miosis. If the 3rd order neuron (the last of 3 neurons in the pathway which ultimately discharges norepinephrine into the synaptic cleft) is intact, then the amphetamine causes neurotransmitter vesicle release, thus releasing norepinephrine into the synaptic cleft and resulting in robust mydriasis of the affected pupil. If the lesion itself is of the aforementioned 3rd order neuron, then the amphetamine will have no effect and the pupil remains constricted. There is no pharmacological test to differentiate between a 1st and 2nd order neuron lesion.
- Dilation lag test
It is important to distinguish the ptosis caused by Horner's syndrome from the ptosis caused by a lesion to the oculomotor nerve. In the former, the ptosis occurs with a constricted pupil (due to a loss of sympathetics to the eye), whereas in the latter, the ptosis occurs with a dilated pupil (due to a loss of innervation to the sphincter pupillae). In an actual clinical setting, however, these two different ptoses are fairly easy to distinguish. In addition to the blown pupil in a CNIII (oculomotor nerve) lesion, this ptosis is much more severe, occasionally occluding the whole eye. The ptosis of Horner's syndrome can be quite mild or barely noticeable.
When anisocoria occurs and the examiner is unsure whether the abnormal pupil is the constricted or dilated one, if a one-sided ptosis is present then the abnormally sized pupil can be presumed to be the one on the side of the ptosis.
- ↑ Adams, Raymond Delacy; Victor, Maurice; Ropper, Allan H. (2001). Adam and Victor's principles of neurology, New York: McGraw-Hill.
- ↑ Gesundheit B, Greenberg M (2005). Medical mystery: brown eye and blue eye--the answer. N Engl J Med 353 (22): 2409-10. PMID 16319395.
- ↑ Horner JF. Über eine Form von Ptosis. Klin Monatsbl Augenheilk 1869;7:193-8.
- ↑ Who Named It synd/1056
- ↑ Graff JM, Lee AG. Horner's Syndrome (due to Cluster Headache): 46 y.o. man presenting with headache and ptosis.. Ophthalmology Grand Rounds. The University of Iowa. URL accessed on 2006-09-22.
Nervous system pathology, primarily PNS (G50-G99, 350-359)
|Nerve, nerve root|
and plexus disorders
cranial nerve: V (Trigeminal neuralgia) - VII (Facial nerve paralysis, Bell's palsy, Melkersson-Rosenthal syndrome, Central seven) - XI (Accessory nerve disorder)
and other disorders of the PNS
| Diseases of myoneural junction|
Myasthenia gravis - Primary disorders of muscles (Muscular dystrophy, Myotonic dystrophy, Myotonia congenita, Thomsen disease, Neuromyotonia, Paramyotonia congenita, Centronuclear myopathy, Nemaline myopathy, Mitochondrial myopathy) - Myopathy - Periodic paralysis (Hypokalemic, Hyperkalemic) - Lambert-Eaton myasthenic syndrome
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