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Horners syndrome

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Horners syndrome

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Horners syndrome

  1. 1. Horner's syndrome Presenter : Dr Rahul Achlerkar Moderator : Dr Atul Seth
  2. 2. Introduction  The term Horner syndrome is commonly used in English- speaking countries, whereas the term Bernard-Horner syndrome is common in France  Horner syndrome (Horner’s syndrome) results from an interruption of the sympathetic nerve supply to the eye
  3. 3. Horner’s  Characterized by the classic triad of  Miosis (constricted pupil)  Partial ptosis  Loss of hemifacial sweating ( anhidrosis).
  4. 4. Neuroanatomy Sympathetic innervation to the eye consists of a 3-neuron arc.  First-order central sympathetic fibers  Second-order preganglionic pupillomotor fibers  The third-order post ganglionic pupillomotor fibers
  5. 5. First-order central sympathetic fibers Arise from the posterolateral hypothalamus Descend uncrossed through the midbrain and pons Terminate in the cell column of the spinal cord at the level of C8-T2 (ciliospinal center of Budge).
  6. 6. Applied Anatomy First-order neuron lesions  Cerebral vascular accident (CVA)/Wallenberg syndrome  Demyelinating disease  (eg, multiple sclerosis)  Arnold-Chiari malformation  Basal meningitis  (eg, syphilis)  Basal skull tumors
  7. 7. First-order neuron lesions  Hemisensory loss  Dysarthria  Dysphagia  Ataxia  Vertigo  Nystagmus
  8. 8. Second-order preganglionic pupillomotor fibers Exit spinal cord at the level of T1 and enter the cervical sympathetic chain They are in close proximity to the pulmonary apex and the subclavian artery. The fibers ascend through the sympathetic chain and synapse in the superior cervical ganglion at the level of the bifurcation of the common carotid artery (C3-C4).
  9. 9. Applied Anatomy  Pancoast tumor  tumor in the apex of the lung, most commonly squamous cell carcinoma  Birth trauma with injury to lower brachial plexus  Cervical rib
  10. 10. Applied Anatomy  Aneurysm or dissection of the aorta  Lesions of the subclavian or common carotid artery  Neuroblastoma  Lymphadenopathy  eg, Hodgkin disease, leukemia, tuberculosis, or mediastinal tumors
  11. 11. Second-order neuron lesions  Prior trauma  facial, neck, axillary, shoulder or arm pain  Cough  Hemoptysis  Previous thoracic or neck surgery  Previous chest tube or central venous catheter placement; or neck swelling
  12. 12. The third-order pupillomotor fibers Postganglionic pupillomotor fibers exit the superior cervical ganglion and ascend along the internal carotid artery Shortly after the postganglionic fibers leave the superior cervical ganglion, vasomotor branch off It Travels along the external carotid artery to innervate the blood vessels and sweat glands of the face.
  13. 13. The third-order pupillomotor fibers Ascending along the internal carotid artery enter the cavernous sinus The fibers then leave the carotid plexus briefly to join the abducens nerve in the cavernous sinus It enter the orbit through the superior orbital fissure along with the ophthalmic branch of the trigeminal nerve via the long ciliary nerves. The long ciliary nerves then innervate the iris dilator and the Müller muscle
  14. 14. Third-order neuron lesions  Internal carotid artery dissection  associated with sudden ipsilateral face or neck pain  Raeder syndrome (paratrigeminal syndrome)  Carotid cavernous fistula  Cluster or migraine headache  Herpes zoster
  15. 15. Raeder’s syndrome  Horner’s with pain in the distribution area of V1.  Caused by a neoplasm compressing the trigeminal nerve.  Differential for cluster headaches.
  16. 16. Third-order neuron lesions  Diplopia from sixth nerve palsy  Numbness in the distribution of the first or second division of the trigeminal nerve and pain
  17. 17. Studies
  18. 18. Etiology  Horner syndrome can be congenital, acquired, or purely hereditary (autosomal dominant)
  19. 19. The interruption of the sympathetic fibers may occur Centrally between the hypothalamus and the fibers’ point of exit from the spinal cord C8 to T2 Peripherally in cervical sympathetic chain, at the superior cervical ganglion, or along the carotid artery
  20. 20.  Drugs that may cause symptoms similar to Horner syndrome include the following:  Acetophenazine  Bupivacaine  Butaperazine  Chloroprocaine  Chlorpromazine  Fluphenazine  Guanethidine  Influenza virus vaccine  Levodopa
  21. 21. Clinical Presentation  Patient history  Obtaining a careful history is very helpful in the localization of lesions causing Horner syndrome.  The symptoms reported by the patient will depend on the site of lesion
  22. 22. differential diagnosis  Anisocoria  Adie pupil  Argyll Robertson pupil  Holmes-Adie pupil (contralateral)  Iris sphincter muscle damage  Senile miosis  Third nerve palsy  Unilateral use of miotic drugs  Unilateral use of mydriatic drugs
  23. 23. Anisocoria Pupillary inequality greatest In bright light (large pupil) In dim light (small pupil) 3rd nerve palsy Trauma Tumor Temporal lobe herniation Aneurysm No 3rd nerve palsy Drug induced Adie’s pupil Iris damage (trauma/surgery/laser) Basal meningitis Ptosis Horner syndrome Physiological
  24. 24. Testing  Which is the abnormal pupil  Compare in light and dark.  Direct and consensual response  Is accomodation affected?
  25. 25. Light Reflex
  26. 26. Normal pupil reaction  video
  27. 27.  Argyll-Robertson pupil  Small, irreg  Does not react to light  Reacts to accommodation  Causes  syphilis  diabetes  Miotonic pupil (Adie’s syndrome)  Dilated  Poor response to light and convergence.  Constricts with weak Pilocarpine  Holmes-Adie syndrome  Reduced tendon reflexes (Knee, ankle) - Orthostatic hypotension Afferent & efferent defects
  28. 28. Adie’s tonic pupil (OD)
  29. 29. Argyll-Robertson pupil
  30. 30. Horner’s pupil (OS)
  31. 31. Pharmacologic Testing  The pharmacologic tests document the presence or absence of an ocular sympathetic lesion and identify the level of involvement (ie, preganglionic or postganglionic)  Localizing the lesion is important because preganglionic lesions are associated with a higher incidence of malignancy that necessitates extensive investigations.
  32. 32. Topical cocaine test  The basis for the topical cocaine test is the ability of cocaine to act as an indirect sympathomimetic agent by inhibiting the reuptake of norepinephrine from the synaptic cleft at the nerve ending
  33. 33. Procedure  The test is performed by instilling cocaine solution (2-4% ) into each eye.  Cocaine instilled in an eye with intact sympathetic innervation causes the pupil to dilate.  A sympathetically denervated pupil ( in Horner syndrome) dilates poorly to cocaine, regardless of the level of the sympathetic interruption, because of the absence of endogenous norepinephrine in the synapse.
  34. 34.  For optimal accuracy, test results should be evaluated 30 minutes or longer after cocaine is administered.  The maximal response is seen 40-60 minutes after instillation of the drops.  Postcocaine anisocoria greater than 0.8 mm is sufficient to diagnose Horner syndrome.
  35. 35. Disadvantages  The drops are difficult to obtain because they must be made at a compounding pharmacy  The drops are relatively expensive  The test can yield equivocal results  Cocaine metabolites may be detected in urine
  36. 36. Topical apraclonidine test  The topical apraclonidine test is a practical and reliable alternative to the topical cocaine test  It is readily available and adequately sensitive (87%) and is currently the test of choice.
  37. 37. Apraclonidine  It is  an ocular hypotensive agent  weak alpha1-agonist  strong alpha2-agonist  Typically given in a 0.5% or 1% solution  It has little to no effect on a normal pupil but has a mydriatic effect on an abnormal pupil
  38. 38.  In Horner syndrome, upregulation of alpha1-receptors increases apraclonidine sensitivity and causes denervation supersensitivity of the iris dilator muscle.  The denervation supersensitivity results in pupillary dilatation and lid elevation on the abnormal side but no response or mild miosis on the normal side from alpha2-activity after apraclonidine administration.  Reversal of anisocoria occurs after bilateral instillation of apraclonidine.
  39. 39.  In acute cases, false-negative test results may occur because the alpha1-receptor upregulation on which the effect of apraclonidine depends may take 5-8 days.  A negative apraclonidine test result especially in acute settings does not exclude Horner syndrome.  In such cases, a cocaine test should be performed to exclude Horner syndrome.
  40. 40. Side Effects  Apraclonidine 0.5% or 1% may cause  Lethargy  Bradycardia  respiratory depression in infants , younger than 6 months  Because of the immaturity of the blood-brain barrier.
  41. 41.  VIDEO
  42. 42. Topical hydroxyamphetamine test  The localization of a lesion causing Horner syndrome may be aided by the use of the topical hydroxyamphetamine test.  Hydroxyamphetamine stimulates the release of stored endogenous norepinephrine from the postganglionic axon terminals into the neuromuscular junction at the iris dilator muscles.
  43. 43.  This test may distinguish a postganglionic third-order neuron lesion from a presynaptic second-order or first-order neuron lesion.  To perform the test, 2 drops of 1% hydroxyamphetamine solution are instilled into each eye.  A period of 24-48 hours must be allowed to elapse between the cocaine test and the hydroxyamphetamine test because cocaine has the ability to inhibit the uptake of hydroxyamphetamine into the presynaptic vesicles,
  44. 44.  Hydroxyamphetamine drops instilled into an eye with Horner syndrome with intact postganglionic fibers (ie, first- or second- order neuron lesions) dilate the affected pupil to an equal or greater extent than they do the normal pupil.  However, hydroxyamphetamine drops instilled into an eye with Horner syndrome with damaged postganglionic fibers (ie, third-order neuron lesions) do not dilate the affected pupil as well as they do the normal pupil.
  45. 45. Treatment & Management  In general, appropriate treatment of Horner syndrome depends on the underlying cause.  The goal of treatment is to eradicate the underlying disease process.  In many cases, however, no effective treatment is known.  Prompt recognition of the syndrome and expedient referral to appropriate specialists are vital.

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