Posts Tagged ‘Horner’s syndrome’

Pupil Examination

Wednesday, August 20th, 2014

Subtitles in English for this video can be displayed by clicking on CC (first button on the bottom right hand corner of the video).

The size of the pupillary aperture at any point in time is dependent on a balance between sympathetic tone, parasympathetic tone, the light reflex and the near reflex.

The light reflex is an important marker for optic nerve function. The afferent pathway of the light reflex is the optic nerve, with each one connecting to the parasympathetic fibers of the oculomotor nerves on both sides to form the efferent pathways. Hence, light shown on one eye causes equal pupil constriction in both eyes. An asymmetrical light reflex, as evidenced by a relative afferent pupillary defect, is an indicator for optic neuropathy.

Technique

  1. The examination should be carried out in dim light, to prevent pupil constriction.
  2. The patient is then advised to fixate on a distant object throughout the examination. This overcomes the near reflex (which also causes pupil constriction). The doctor stands towards the side of the patient when performing the test.
  3. Pupil symmetry: First, the torch is shone equally on both eyes from below to look for pupil asymmetry. Avoid direct light into the eyes to prevent excessive pupil constriction. Now repeat the test with the room light at its brightest. If the asymmetry is most marked in dim room light (scotopic conditions), then the smaller pupil is the abnormal one. If the asymmetry is most marked in bright room light (photopic conditions), then the larger pupil is the abnormal one.
  4. Direct and consensual light reflexes: Next, light is directly shone on one eye for 3 seconds, and pupillary constriction is assessed in both eyes. Constriction of the pupil in the tested eye is called a direct light reflex, whilst constriction of the pupil in the non-tested eye is called a consensual light reflex. Failure for both pupils to constrict indicates an absolute afferent pupillary defect of the tested eye, which is only seen in catastrophic optic nerve damage (i.e. optic nerve transection). Failure of one of the two eyes to constrict to light indicates abnormalities with the efferent pathways or the iris sphincter. (see Pupil Exam video).
  5. Swinging torch test: To uncover less severe forms of optic nerve damage, pupil constriction is compared between both eyes using a swinging torch test. The pre-requisite for the test is that optic nerve damage is unequal or unilateral. First shine the torch on one eye for 3 seconds, then quickly move to the next eye and remain in place for 3 seconds, then continue switching from one eye to the other in rapid succession. Stimulation of the normal eye should elicit a brisk constriction of both pupils but when the light is shone on the diseased eye, both pupils dilate. What happens is that the dilatation produced by withdrawing the light from the normal eye outweighs the weak constriction produced by shining light on the diseased eye. This is known as a relative afferent pupillary defect.

Clinical importance

Pupil asymmetry

Also known as anisocoria. The presence of this indicates an imbalance between pupil dilator (sympathetic) and constrictor muscles (parasympathetic). Before considering the possible neurological causes, it is important to take a history of previous ocular conditions (including acute glaucoma, uveitis), ocular trauma and ocular surgery (cataract surgery), as damage to the iris muscles can cause abnormalities in pupil size.

For a unilateral dilated pupil, the most important condition to look for is an oculomotor nerve palsy. Other signs to look for include ipsilateral ptosis, squint (the eye is deviated downwards and outwards). In pupil-involving oculomotor nerve palsy, it is vital to consider a space-occupying lesion (such as an aneurysm) compressing on the nerve on its route from the brainstem towards the eye.

For a unilateral constricted pupil, the most important condition to look for is Horner’s syndrome. The sympathetic nerve supply begins at the hypothalamus. The preganglionic neurons travel down the brainstem, and then along the lung apex towards the superior cervical ganglion. This lies deep to the sheath of the internal carotid artery and internal jugular vein at the level of the second and third cervical vertebrae. The postganglionic neurons then travel along the internal carotid artery towards the eye. Other signs to look for include ipsilateral partial ptosis, relative enophthalmos and occasionally anhidrosis. A confirmatory test is 4% cocaine drop test. Cocaine blocks the reuptake of noradrenaline at synaptic cleft. In Horner’s syndrome there is a lack of noradrenaline at the synaptic cleft due to loss of innervation. A positive sign is where the pupil fails to dilate to 4% cocaine solution. The most important lesion to look for is a pancoast tumor: bronchogenic carcinoma of the lung apex. A chest X-Ray may reveal an otherwise asymptomatic lung lesion.

Relative afferent pupillary defect

Also known as a Marcus Gunn pupil. A paradoxical dilation of the pupil when a bright light is swung towards an eye indicates a positive relative afferent pupillary defect. Conditions to consider include lesions of the optic nerve, optic chiasm, optic tract as well as diffuse/severe retinal diseases. This is distinguished from a complete optic nerve lesion, where the pupil fails to constrict to light at all. To identify a relative afferent pupillary defect the efferent pathway must be intact. Hence anisocoria is absent during initial pupil assessment.

Common mistakes in examinations

  1. Completely switching off all room lights, causing temporary confusion amongst all parties present.
  2. Standing directly in front of the patient, inducing a near reflex.
  3. Forgetting to check consensual light reflexes.
  4. Moving the torch too slowly between eyes during the swinging torch test. This allows the pupil adequate time to dilate, thus giving a false positive result of a relative afferent pupillary defect.

Horner’s Syndrome

Wednesday, August 20th, 2014

The patients in these two photos show the classical signs of Horner’s syndrome. In the first photo (Figure 1), there is left-sided partial ptosis, miosis and anhidrosis. Whilst in the second photo (Figure 2), there is right-sided ptosis and miosis.

Horner’s syndrome is caused by a lesion affecting the sympathetic pathway. This pathway starts as the 1st order sympathetic neuron which originates from the hypothalamus, travelling along as sympathetic fibres in the brainstem and terminates at the C8-T1 level of the spinal cord. The first-order neurons then branch with second order neurons (pre-ganglionic tract), which travels a long intra-thoracic course from the C8-T1 level of the spinal cord to the superior cervical ganglion at the level of C2. Finally, the cervical sympathetic pathway continues as third order neurons (post-ganglionic tract) which travels from the cervical ganglion at the level of C2, along the carotid artery, through the superior orbital fissures, cavernous sinus, orbital apex and finally terminates by supplying the levator palpebrae superioris muscle, superior tarsal muscle and the pupillary dilator muscles. Branches from the 3rd order sympathetic neurons also supply the sweat glands and blood vessels of the face. As the function of the levator palpebrae superioris and superior tarsal muscles include raising the upper eyelid, and the pupillary dilator muscles is involved in dilation of the pupil, patients with Horner’s syndrome may therefore present with partial ptosis and miosis.

Any lesion affecting the 1st, 2nd and 3rd order cervical sympathetic neurons may result in Horner’s syndrome and common causes would include: 1) brainstem stroke causing lateral medullary syndrome, 2) Pancoast’s tumour affecting the lung apex, 3) thoracic aortic aneurysm, 4) carotid artery dissection, 5) cavernous sinus pathologies and 6) local eye pathologies.