Horner’s Syndrome

  • Caused by interruption of the ipsilateral sympathetic outflow to the head and neck.
    • Three neuron sympathetic outflow path must be intact to provide tonic output of norepinephrine at the effector cell.
      • Central cells origin in hypothalamus.
      • Axons traverse brainstem to spinal cord levels C7-T1.  Axons from intermediolateral  spinal column of the spinal cord provide 2nd step in the three-neuron arc.
      • From the spinal cord and beyond, the fibers form part of the peripheral nervous system.
        • Fibers proceed across the apex of the lung.
        • Fibers ascend to C3-C4 superior cervical ganglion, where they synapse and travel with the internal carotid artery into the cavernous sinus.
        • Sympathetic fibers join the abducens nerve, and then enter the orbit with the ophthalmic branch of the trigeminal nerve.

 

 

Horners

  • The combination of miosis and ptosis by itself is not particularly helpful in localizing the lesion.
    • It can result from lesions in the brainstem or spinal cord, damage at the lung and in the supraclavicular space, or damage to the carotid plexus along the internal carotid artery all the way to the cavernous sinus.
  • Clinical signs
    • Ptosis
      • Muller’s muscle-the sympathetically innervated retractor of the upper lid, is paralyzed in Horner’s syndrome, and this narrows the palpebral fissure.
      • The lower lid is has some sympathetically innervated fibers-causing some “upside down ptosis”
    • Miosis
      • Tiny pupil-is never intense
      • Paralysis of pupillodilator muscle causes only moderate decrease in the pupil size
    • Dilation lag
      • The slowness of the affected pupil to dilate is characteristic of Horner’s syndrome.
      • Can be of great clinical help in making the diagnosis.