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Amsler Grid

2009-03-06T04:58:00.000-08:00

Hi,

This video is a brief explanation of how and when to use an amsler grid. The Video is designed to display as an amsler grid when viewed with an iphone or ipod touch, when this audio commentry can be muted out.

An amsler grid is simply a grid of 5mm squares, with a central fixation dot in the middle. A normal grid is 10cm wide by 10cm high. To print one out just google amsler grid pdf.

It is used to detect distortion or blind spots called scotoma in the central vision, And this is most commonly used to detect and monitor for changes associated with Age Related Macular Degeneration or AMD.

The grid should be held at a normal reading distance of approximately 30cm, with one eye covered while the other is tested. Reading glasses should be worn. While fixing upon the central dot, the patient is asked whether any part of the grid is either distorted or missing.

If there is distortion or gaps in the grid, this could suggest a problem with the macular area of the retina and should be seen by an eye specialist. People who are aleady known to have AMD can use this grid to check that any blind spot or distortion are not changing over time.

Monitoring for early signs of AMD has become more important in the last couple of years with the availability of effective treatments for Wet AMD. This is the type of Macular Degeneration associated with development of new blood vessels within the macula. If treated early these new blood vessels can regress before they are able to cause permanent scarring and damage to the vision. New symtoms should therefore be seen urgently by a specialist within a few days where possible.

Visual Fields

2009-03-06T04:57:00.000-08:00

Hi,

Our field of vision is the total area we are able to see, and is the combination of the individual visual fields of our 2 eyes. When looking straight ahead a normal field extends about 60 degrees up, 75 degrees down, 60 degrees nasally and an impressive 110 degrees temporally. The overlapping areas represent binocular vision, where depth perception or stereopsis is possible.

The shape of the field of each eye is rather like the shape of a pair of sunglasses. For simplicity the field of each eye can be documented as an oval shape, with the visual field of the right eye drawn on the right side of the page and the left eye on the left side. This is as if the patient is looking out through the page you have in front of you. For example a patient who could not see below the horizon from his right eye would be documented like this, with the dark area representing the area the patient is unable to see. You should notice that this is different from how you would record a scar on the right side of a patients face, where the drawing would be as if the patient was sitting in front of you. This reversal of sides when recording visual fields can cause confusion, so remember that fields are drawn the wrong way round, compared with the rest of the notes, and make sure you label them accordingly. This is a right inferior altitudinal defect.

The visual pathway is the wiring from the eye to brain, with the destination being the primary visual cortex in the occipital lobes, also known as the striate cortex. Damage along this pathway causes characteristic field defects. This pathway starts in the eye with the rod and cone photoreceptors in the retina. These synapse via bipolar cells with the ganglion cells of the retinal nerve fibre layer. These unmyelinated fibres pass into the optic disc and become myelinated as they become the optic nerves. We all have a small blind spot or scotoma corresponding to the optic disc which lacks photoreceptors. This physiological scotoma is slightly to the side or temporal to the centre of our vision.

Damage to the macula area of retina causes loss of central vision or central scotoma, seen most commonly in age related macular degeneration or AMD. An Amsler grid is a simple 5mm grid pattern, where the patient attempts to fix at the central dot from about 30cm with each eye in turn. These can be useful to identify and monitor central scotoma.

A new or changing central scotoma or indeed distortion of central vision may indicate treatable Wet AMD, and should be seen promtly by an eye specialist. Damage to the nerve fibres as they pass through the optic disc is seen in glaucoma. These defects cause an arcuate scotoma which follows the pattern of the nerve fibre layer. Here an upper nerve fibre layer defect causes a lower arcuate scotoma. Later this can extend to an upper or lower altitudinal defect, then complete loss of peripheral field and finally blindness. Identification of early glaucoma field defects can allow treatment to delay or prevent this progression, and preserve vision. As well as the visual field, assessment of glaucoma features the appearance of the optic disc, the Intraocular Pressure and the medical history.

The optic nerve function can be affected in many ways, for example in thyroid eye disease it can be compressed, In optic neuritis it can be inflamed and in Giant cell arteritis it can be ischaemic. These may cause various shapes of field defect such as an altitudinal defect or a mixed field defect which does not respect the horizontal or vertical midline. These causes mentioned can affect one or both eyes at the same time.

The optic chiasm is named after the greek letter chi or X. At this crossing the signal from each eye is split in two, with the nasal retinal fibres crossing sides, while the temporal retinal fibres stay on the same side. The effect of this selective crossing is that the vision corresponding to the left hand field of view is supplied to the right hand side of the brain, with the right visual field going to the left brain. So the right brain controls the left hand, and the right brain sees the left field of vision from both eyes. Compression of the chiasm, most commonly by a pituitary tumour can cause a bitemporal hemianopia, with only the crossing fibres are affected. In the early stages these field defects may be missed, sometimes for years. In practice these defects are neither complete nor symmetrical.

Beyond the chiasm is the optic tract which terminates in the lateral geniculate nucleus in the thalamus. From here fibres fan out into the optic radiations which synapse in the striate cortex. Defects beyond the chiasm, the so-called retrochiasmal pathway, cause homonymous defects, meaning a similar area of the field is affected in both the eyes. It is important to note that the vertical midline is never crossed.

The optic radiations are also called the geniculo-calcarine tract. Damage to this tract occurs most commonly due to stroke and can cause quadrantanopia or hemianopia depending upon lesion size. Temporal lobe lesions cause superior quadrantanopia, or pie in the sky, and may have associated complex partial seizures, memory problems or Wernicke's aphasia if dominant hemisphere. Parietal lobe lesions cause inferior quadrantic defects or pie on the floor, with possible associated sensory disturbances and Gerstmanns and aphasic syndromes if dominant hemisphere.

Homonymous hemianopia and quadrantanopia most commonly arise from occipital strokes affecting the striate cortex. Posterior cerebral artery infarcts with intact middle cerebral collateral perfusion may cause so-called macula sparing, where the hemianopia spares the central vision.

Visual inattention is common in stroke patients and may mimic or accompany homonymous hemianopia. With visual inattention the visual pathway may be intact, but the patient fails to notice the vision on the affected side. This can be demonstrated by offering the patient simultaneous bilateral stimuli.

So how should visual fields be assessed? Well this depends upon the context of the examination. So far we have looked at field defects as being absolute, they are either present or absent. In practice the visual field is like and island of vision, with the centre of the vision being most sensitive. This means a small or dim target can be detected centrally just as easily as a bright or large target peripherally. Accurately mapping the shape of this island of field allows for early detection of problems, and to demonstrate changes over time. Two machines are in common use in the UK to assist with this, first is the humphrey field analyzer, second is the goldmann visual field. Both machines sit the persons face inside a bowl of uniform light.

The humphrey machine typically only measures the central 24 or 30 degrees of field. This makes it unsuitable for early detection of compression of the optic chiasm. One eye is covered while the other fixates upon a central target. Lights of various brightness are shown across a grid pattern within the bowl until the threshold for detection of the light is established at each point. When the person sees the light flash, they press a button. The results are printed as a numeric value for the sensitivity at each point, and then represented as a grey-scale picture to aid interpretation. This is typically used for screening and monitoring of glaucoma. Here is a normal Humphrey field, while here is an arcuate defect in glaucoma. This is termed static threshold perimetry as the stimuli are shown in fixed grid positions to establish the threshold at each point.

In contrast the Goldmann Field is kinetic threshold perimetry, where the light stimulus is moved in towards the centre of vision until it is detected. The patient again fixes the tested eye upon a central light target, while this time an examiner manually brings lights towards the centre of vision until it is detected. These points are then plotted into isopters like contour lines on a map. By repeating with differcnt light brightness or size the 'shape' of the field is plotted. The goldmann field can be measured out to 90 degrees, and is most commonly used to monitor neurological field changes. For example before and after treatment of a pituitary tumour.

Finally we have field testing to confrontation. In an asymptomatic individual I think this should be a brief screening examination taking a few seconds. I check central vision, four quadrants and temporal field. If they are a possible stroke patient, begin by checking for inattention.

First ask the patient cover one eye and look at my face. Then ask them to tell you if any part of the vision is missing. If the patient thinks it is all present, then usually they have normal fields. If they cannot see part of your face, then use an amsler grid to check their central vision for distortion and scotoma. Patients may use this grid to monitor their central vision at home.

Next the four quadrants. Again with one eye covered. Ask a patient to look you in the eye and tell you if they can see your finger wiggling in each quadrant. If they cannot see part, then it can be mapped out more carefully with a red hat pin, particularly noticing whether it crosses the horizontal or vertical midline. Finally, for peripheral field I ask a patient whether they can see a finger wiggle at 90 degrees to each eye, about 5cm away.

Of course more detailed examination is possible, but I think the most likely reason to miss a field problem is not because of a brief examination, but because the fields are not examined at all.

So lets wrap up.

Central loss of field is most common in macular degeneration, and should be assessed by and eye specialist, urgently if recent in onset. Field defects which respect the horizontal midline arise from the eye or optic nerve. Causes include glaucoma, branch retinal vein occlusion, optic neuritis, optic nerve ischaemia. They should be assessed by an eye specialist. Field defects which respect the vertical midline may arise from the optic chiasm and beyond. Causes include stroke and brain tumours. Humphrey field testing is routinely used to screen and monitor glaucoma, while goldmann testing may be used in neurological field defects.
Examination to confrontation can be done quickly, so that it need not be missed out of any routine neurological or ophthalmological assessment

Actions of the ocular muscles

2009-03-06T04:54:00.000-08:00

Hi,

Understanding the actions of the extraocular muscles can be frustratingly confusing, so i hope this video helps. You may also want to watch the video on eye movement terminology before this one.

The eye sits within the bony orbit. The orbit has a roof, a floor, a medial wall and a lateral wall. It is therefore somewhat pyramid like in shape.

The two orbits have medial walls that run parallel to one another. The lateral walls are at about 45 degrees to the medial wall, or 90 degrees to each other.

The eye sits within the middle of this space, with the 4 recti muscles converging on the orbital apex, where they insert into the annulus of zinn, a fibrous ring of tissue that encircles the optic nerve.

These recti are superior rectus, medial rectus and inferior rectus, all supplied by the oculomotor or 3rd cranial nerve, and lateral rectus supplied by the abducens or 6th cranial nerve.

The inferior oblique is also supplied by the oculomotor nerve while the superior oblique is supplied by the trochlear or 4th cranial nerve.

Contraction of the lateral rectus abducts the eye while contraction of the medial rectus adducts the eye. The two opposing muscles are described as being antagonists. Sherringtons law of reciprocal innervation states that when a muscle is stimulated, its antagonist is inhibited. This means that abduction is a combination of contraction of the lateral rectus and relaxation of the medial rectus.

As well as have an antogonist muscle, there is also a yoke muscle, which achieves the same movement in the other eye. So for right gaze or dextroversion, the lateral rectus abducts the right eye, and the medial rectus adducts the left eye. Herrings law states that the yoke muscle receives equal and simultaneous innervation, the magnitude of which is determined by the fixing eye.

When the eye is abducted 23 degrees the superior and inferior recti are aligned with the axis of the eye. They therefore act purely to elevate and depress the abducted eye. The superior oblique acts to intort and the inferior oblique acts to extort.

When the eye is adducted, the inferior oblique and superior oblique become the main elavator and depressors. The superior rectus now primarily intorts and inferior rectus primarily extorts.

How can you remember these eye movements?

I draw a simple diagram:

This diagram shows the abducted eye due to lateral rectus, with elevation from superior rectus and depression from inferior rectus. It also shows Adduction from medial rectus with elevation from inferior oblique and depression from superior oblique.

Finally for the intortion and extortion simply turn the eyebrows into arrows. The superior rectus and superior oblique muscle are both intorters.

Eye Movement Terminology

2009-03-06T04:53:00.001-08:00

Hi

this short video is to introduce terminology of eye movements. These are in 3 groups, ductions, versions and vergences.

DUCTIONS

First we will consider movements of a single eye alone, or Ductions.
We will face a patient with the eyes pointing straight ahead, this is called the primary position.
Now we cover or occlude the patients left eye, to observe ductions of the right eye.
movement of the cornea away from the midline is abduction, movement towards the midline is adduction.
movement upwards is supraduction or elevation and downwards is infraduction or depression.
rotation of the upper cornea towards the midline is incyclotorsion or intorsion, and rotation away is excyclotorsion or extorsion.

VERSIONS
Next we have conjugate eye movements in different directions of gaze. These gaze movements are termed versions.
Dextroversion is gaze to the right. The right eye is abducted and the left is adducted.
Laevoversion is gaze to the left. The right eye is now adducted with the left abducted.
upgaze and downgaze are supraversion and infraversion, although the terms upgaze and downgaze are also used.
Finally there is dextrocycloversion where the upper corneas move to the right and laevocycloversion where they move to the left.

VERGENCES
Finally we come to Vergences, here we have convergence, with both eyes adducted, and divergence where both eyes abduct back to the primary position.
There is also incyclovergence and excyclovergence.

So isolated movements of a single eye are descibed as ductions
Conjugate gaze movements of both eyes are versions.
Vergence movements are mirror image movements, being equal and opposite.
Both version and vergence movements can be described as combinations of ductions of the two eyes.

Anisocoria

2009-03-06T04:52:00.001-08:00

Hi,

Difference in pupil sizes is termed anisocoria.

Based on clinical findings, it can be divided into 3 groupings.

First is an abnormally large pupil. This is obvious in normal lighting but less so with the lights off, because the other normal pupil dilates.

Next is an abnormally small pupil. This may not be visible in normal lighting, but with the lights off becomes obvious due to dilation of the normal pupil.

Finally is pupil aysmmetry up to 2mm that doesn't change in light and dark. Both pupils change size, but the relative difference remains the same. This is present in up to 20% of normal people and termed physiological anisocoria. Both eyes respond normally to light.

Back to the abnormally large pupil termed a mydriasis. The autonomic nervous system controls pupil movement, with constriction supplied by the parasympathetic fibers which travel with the 3rd cranial nerve. Loss of the parasympathetic signal causes the pupil to dilate.

Look, therefore, for diplopia or ptosis to suggest a 3rd nerve palsy. This can be caused by berry aneurysm compressing the 3rd nerve, which can accompany and occasionally precede subarachnoid haemorrhage. Here the affected right eye is dilated, down and out, with a ptosis.
A dilated pupil without ptosis or diplopia is unlikely to arise from a 3rd nerve palsy. See the video on 3rd nerve palsy.

Another cause may be Adies tonic pupil. This is characterized by a dilated pupil, with little response to light, but which may slowly constrict to accommodative effort and relax slowly as well. Adies pupil is presumed to be a postviral denervation of the pupil sphincter and is common in young women. Slit lamp examination may reveal segmental paralysis and flattening of the pupil border, giving rise to a pupil with an irregular shape. There may also be a vermiform movement of the non-paralyzed sections of the iris, literally a worm like constriction effort.

Adie's pupil is confirmed by testing with dilute pilocarpine 0.125% eyedrops which shows constriction within 20 minutes, but this denervation supersensitivity usually takes some weeks to develop after onset of the adies pupil.

Althought a tonic pupil is typically idiopathic, they may arise in diabetes, giant cell arteritis and syphilis where they are usually bilateral, small and termed argyll-robertson pupils.

Blunt trauma to the eye may tear the pupil sphincter and cause a permanently dilated pupil, clinically similar in appearance to an adie's pupil. Diplopia after trauma is suggestive of a blowout fracture. Acutely look for an associated hyphaema and later for angle recession or retinal dialysis. Previous eye surgery may also have damaged the pupil.

Acute glaucoma features a fixed mid-dilated pupil with brow ache, blurred vision and nausea or vomitting. The cornea is hazy on slit-lamp examination, with a very high intraocular pressure.

Finally the commonest cause of a dilated pupil is exposure to dilating drugs. Examples include the eydrops atropine, cyclopentolate and tropicamide. Atropine may dilate a pupil for up to 2 weeks. Gardeners may inadvertently expose themselves to atropine when cutting back the deadly nightshade or bella donna plant. They present with a dilated pupil, blurred vision and slight photophobia. The pupil is widely dilated, and doesn't respond to pilocarpine 1%, but resolves over several days.

Now to the abnormally small pupil. Autonomic control of pupil dilation is by the oculosympathetic pathway. This arises in the hypothalamus, descends the brainstem and cervical spinal cord, ascends the cervical sympathetic chain, the carotid plexus and passes through the cavernous venous sinus with the ophthalmic branch of the trigeminal nerve. Damage along this pathway is termed a horner's syndrome and features a small pupil or meiosis, slight ptosis and loss of sweating or anhidrosis on one side of the face. Confirmatory testing with Apraclonidine drops reverses the anisocoria and often the ptosis too. See the video on horner's syndrome for more details. Causes of a horner's syndrome include carotid artery dissection, which is both life threatening and treatable with anticoagulation.

Other causes of a small pupil are current or previous iritis and current or previous use of pilocarpine eye drops.

Some key points once more.

Anisocoria may arise due to a lesion impairing the efferent sympathetic or parasympathetic pathway to the eye, or due to factors within the eye itself.
The pupils should be examined in both light and dark, with distance fixation.
Ask about eye trauma or surgery, use of eye drops, and gardening.
With a dilated pupil, check for ptosis, diplopia, and response to dilute and 1% pilocarpine.
With a small pupil, confirm horners syndrome with apraclonidine and investigate further urgently

3rd Nerve Palsy

2009-03-06T04:51:00.001-08:00

Hi,

Today I am looking at assessing a patient with a new onset 3rd cranial nerve palsy, also called an oculomotor nerve palsy.

So what are the clinical features?

Well the oculomotor nerve supply's the levator palpabrae superioris muscle, responsible for elevating the upper eyelid.
It also supply's 4 of the 6 extraocular muscles: superior rectus, medial rectus, inferior oblique and inferior rectus. It has no sensory action.
Loss of function of the 3rd nerve therefore causes the remaining lateral rectus and superior oblique muscles to act unnapposed and deviate the eye down and out.
It also carries parasympathetic innervation to the pupil, responsible for pupil constriction. A palsy may therefore leave the pupil dilated. This pupil involvement is typically spared in microvascular palsy.
Finally the deviated eye is hidden behind the drooping or ptotic eyelid due to loss of levator function. This ptosis may relieve the unpleasant diplopia caused by the deviation of the affected eye.

Lets look at the pathway of the oculomotor nerve.

If we look at the brainstem from the side, through the temporal lobe, the oculomotor nerve nucleus lies at the level of the superior colliculus in the midbrain. The nerve exits ventrally, as the subarachnoid portion, into the cavernous sinus where it splits into superior and inferior branches before entering the orbit through the superior orbital fissure.

In section, the oculomotor nerve nuclei lie centrally, close to the midline. The superior rectus subnucleus is distinct in supplying the contralateral eye, while there is a single midline subnucleus supplying both levator muscles. Dorsal midbrain infarction may therefore cause an ipsilateral 3rd nerve palsy with in addition a contralateral upgaze palsy and partial ptosis. The infarct may be visible on MRI.

Pretectal nuclei lie dorsally and receive innervation from the optic tracts as part of the pupil light reflex. These then pass fibres bilaterally to the edinger-westphal nuclues, which is the parasympathetic nucleus responsible for pupil constriction and closely related to the oculomotor nucleus. Fibres from both pass ventrally through the red nucleus and cerebral peduncles and exit as the fascicular subarachnoid oculomotor nerve. Lesions affecting the red nucleus or cerbral peduncles cause ipsilateral flapping tremor or contralateral hemiplegia respectively. Both are easily detected by asking the patient to stretch out their arms.

The parasympathetic fibers run superficially within the nerve and as mentioned are typically spared by microvascular ischaemia which is a common cause of oculomotor nerve palsy in diabetics. Pain in and around the eye is quite common, but neck stiffness or decreased consciousness are not features. The palsy evolves over a period of around 3 days, shows improvement within 4 weeks and has completely resolved within 4 months. A painless 3rd nerve palsy with pupil sparing should make the possibility of ocular myasthenia a consideration where the patient is not diabetic. Check blood pressure, fasting glucose, ESR and a CT head in patients under 50. Re-examine the patient in 1-3 days if the symtoms are less than 48 hours duration, to check the pupils remain normal.

The circle of willis lies immediately beside the subarachnoid oculomotor nerve, with supply from the single basilar artery and two internal carotid artery's. The major branches of these are the anterior cerebral, middle cerebral and posterior cerebral artery's. These are connected into a circle by the single anterior communicating artery - which is the most common site of berry aneurysm, and the two posterior communicating artery's. Posterior communicating artery aneurysms occur at the origin of the artery from the internal carotid and compress the adjacent oculomotor nerve, especially upon rupture with subarachnoid haemorrhage. The patient presents with severe headache, reduced consciousness, neck stiffness and vomiting. The associated oculomotor nerve palsy is isolated, may take 3 days to maximise but normally becomes complete and pupil dilation is the rule. Formal angiography is indicated to exclude aneurysm in all isolated oculomotor nerve palsys with a dilated pupil, with MR angiography an option where the index of suspicion is lower, for example an otherwise well diabetic patient with an oculomotor nerve palsy and slight pupil dilation.

The subarachnoid portion of the 3rd nerve is also vulnerable to basal meningeal infection, inflammation or neoplastic infiltration and these usually affect multiple cranial nerves.

Next the oculomotor nerve enters the cavernous venous sinus. This dural sinus lies beneath the frontal lobes of the brain, with the temporal lobes laterally. The sphenoid sinus lies inferiorly and the pituitary gland sits in the middle within the sella turcica. The optic chiasm crosses in front of the pituitary stalk and the internal carotid artery's loop through the sinus. Laterally the oculomotor nerve sits against the lateral wall, as do the 4th nerve and upper 2 branches of the trigeminal nerve. The Abducens nerve is more medial and is most often the first nerve to be affected by cavernous sinus pathology. Lesions here tend to affect multiple cranial nerves although a 4th or 6th nerve deficit can be difficult to demonstrate clinically when combined with a 3rd nerve palsy. Therefore particular attention should be paid to features suggestive of trigeminal nerve involvement. This would be burning pain and numbness affecting the forehead or cheek, representing the first or second division of the trigeminal nerve. Pupil involvement here is variable, with both sympathetic and parasympathetic pupillary fibres present. The pupil may therefore be small, large or normal. Causes of cavernous sinus lesions include Tolosa-Hunt granulomatous inflammation, Pituitary, Nasopharyngeal or Metastatic Neoplasms and Intracavernous aneurysms. Herpes zoster may also affect the oculomotor nerve, associated with ophthalmic shingles.

Finally the 3rd nerve enters the orbit as superior and inferior branches through the superior orbital fissure and may be damaged by orbital fractures. The superior branch supply's levator and superior rectus, the inferior supplying medial rectus, inferior oblique, inferior rectus, pupil and ciliary muscle. A partial 3rd nerve palsy affecting one of these branches may be a feature of oculomotor palsy elsewhere along its path, and doesn't necessarily localise pathology to the cavernous sinus or orbit. Pathology within the orbit usually also features an abduction deficit, as well as proptosis, lid swelling, conjunctival injection, and chemosis.

Assessment and follow-up of oculomotor nerve palsy is usually by an ophthalmologist in conjunction with orthoptists, who as well as measuring the degree of deficit, may prescribe prisms to control diplopia during recovery.

A few key points once more:
The oculomotor palsy is characterized by unilateral ptosis and an eye that is down and out.
Pupil dilation suggests compression, possibly by berry aneurysm.
A contralateral ptosis or upgaze palsy suggest a dorsal midbrain lesion.
An ipsilateral ataxia or contralateral hemiparesis suggesting ventral midbrain lesion, check by asking the patient to stretch out their arms.
Check for facial parasthesia, corneal sensation, and ask about burning facial pain or numbness to consider cavernous sinus lesions.

How to Examine Horner's Syndrome

2009-03-06T04:47:00.000-08:00

Hi,

Motor supply of pupil movements is by the autonomic nervous system, with the sympathetic nervous system supplying the pupil dilation, and the parasympathetic system controlling constriction.

A defect of the sympathetic supply to the eye, also called an oculosympathetic palsy is horner's syndrome.
It makes the affected pupil smaller or meiotic, causing the pupils to be unequal in size. This pupillary size difference is termed anisocoria.

Here, the right pupil is slightly smaller than the left. When the lights are switched off this anisocoria becomes more obvious as the normal left pupil dilates. The affected right pupil may also dilate, but more slowly, this is called a dilation lag. The anisoria may therefore be greatest a few seconds after switching off the room lights.

Another feature of horner's, illustrated here, is an upper and lower lid ptosis, making the upper and lower eyelids slightly closer together and making the eye appear smaller. The patient may also notice a loss of sweating on one side of the forehead or face, called anhidrosis.

We therefore have a triad of ptosis, meiosis and anhidrosis.

If the horner's syndrome is congenital, or occasionally if longstanding, then iris heterochromia may also be noted. The affected iris being lighter in colour than the other eye.

Horners syndrome can be confirmed pharmacologically by use of apraclonidine 0.5%, commercially available as iopidine drops. First measure the pupil sizes - this is readily acheived by taking a quick photo with a digital camera. Then instill a single drop of apraclonidine into each eye. After 1 hour re-examine the pupils. Horners syndrome is confirmed if the anisocoria is reversed, since apraclonidine has no affect on the normal pupil, but dilates the affected pupil. The ptosis may also disappear. Care is needed with infants under 6 months, as they have been reported to become very lethargic after this test.

An alternative test is the Cocaine 4% test. Here a single drop is instilled in each eye and the eyes re-examined after 1 hour. The cocaine dilates the normal pupil but has little or no effect on the horner's pupil. The anisocoria is therefore increased, most noticeably in light conditions.

Having now diagnosed a horners syndrome, we need to try to locate the cause.
This is divided into 3 groups along the oculosympathetic pathway. Central, preganglionic and postganglionic. It does not cross sides along its entire course.

The central pathway arises at the hypothalamus, then travels down the brainstem and cervical spinal cord to synapse at the ciliospinal centre of budge between C8 and T2. Central horners syndromes are usually not an isolated clinical finding, instead they are part of a wider clinical picture featuring other brainstem or spinal symptoms and signs. Causes of central lesions include stroke, tumour, syrinx, vascular malformations, trauma or demyelination. An example is Lateral Medullary or Wallenberg Syndrome, caused by Posterior Inferior Cerebellar Artery Ischaemia. This features dysphagia, analgesia in ipsilateral face and contralateral trunk and extremities, ipsilateral cerebellar ataxia, and rotary nystagmus; skew deviation may occur, with vertical diplopia. Suspected central lesions are usually investigated by imaging with MRI.

From the ciliospinal centre the second order neurone leaves the spine and joins the sympathetic chain close to the lung apex and passes up to synapse at the superior cervical ganglion in the neck. This preganglionic pathway is damaged in a number of ways. The T1 nerve root may be damaged at birth, with an associated brachial plexus palsy causing hand weakness, termed a klumpke palsy. Compression at the pulmonary apex may arise from pancoast lung tumour or breast cancer and also, TB, cervical rib or vascular anomolies. There may be associated shoulder tip or arm pain where the brachial plexus is affected. This presentation would indicate the need for a Chest X-ray and appropriate referall. Neck surgery or trauma may also injure this preganglionic part of the pathway.

The postganglionic pathway passes from the superior cervical ganglion onto the carotid plexus. It ascends with the internal carotid artery to the cavernous sinus. Here the fibres join the ophthalmic branch of the trigeminal nerve passing through the superior orbital fissure into the orbital apex and becoming the long ciliary nerve before entering the eye. Sweating is not usually affected by postganglionic horners lesions due to divison of the nerve supply at the carotid bifurcation. A horner's syndrome associated with unexplained neck or facial pain should be considered as a carotid dissection and promtly investigated usually by MR Angiography.

A horner's syndrome associated with a gaze palsy should lead to investigation of the cavernous venous sinus region, usually with an MRI.

Cluster headache often features transient horner's syndrome during the attack. Men are affected 6 times more than women. Features of cluster headache are severe headache around the eye or temple associated with lacrimation and redness, blocked or watering nose and sweating all on the one side. The attacks last 30 minutes to 2 hours, are often 1 to 2 times per day and after 4 - 8 weeks they stop, on average for around a year. They are both debilitating and treatable, with verapamil and steroids effective for prophylaxis.

How to examine RAPD

2009-03-06T04:45:00.000-08:00

Hi,

Today we are looking at Relative Afferent Pupil Defects, or RAPD. This is also sometimes referred to as Marcus-Gunn pupil.

First we will compare its clinical appearance with that of normal pupils and also that of a complete afferent pupil defect.

To avoid pupil constriction while accommodating, ask to the patient to fix on a distant object throughout your examination.

Look for equal pupil sizes, and check again with the lights off. Anisocoria is not a feature of an afferent defect.

Now check for a reaction to light in each eye, again with the lights off. Here the normal pupils constrict briskly, then relax a little. They dilate again after the light is removed.

now swing the light from eye to eye, quickly - but pausing on each eye for around 2 seconds. In the normal patient the pupils will constrict then relax a little each time the light is swung to them.

Now a patient with a relative afferent defect. The pupils will be equal size in both light and dark. Both pupils will react to light, although sometimes a slower response is noted when light is shone on the affected side.

With the swinging light test the RAPD now becomes obvious. On the affected side, both pupils dilate when the light is swung across. Here the left side is affected.

You will miss an RAPD if you do not do the swinging light test, as it is only by comparing the relative strengths of the signals reaching the brain from the eyes that the abnormality is detected.

Finally with a complete afferent pupil defect, there is no pupil reaction to light shone on the affected side.

Due to crossing of nerve fibres at the optic chiasm, an RAPD localizes pathology to the visual pathway before the chiasm, that is the optic nerve or retina.

Some examples of pathologies causing an RAPD are Large Retinal Detachment, Central Retinal Artery or Ischaemic central retinal Vein Occlusion, Optic Nerve Ischaemia, Optic Neuritis, asymmetric glaucoma

It should be noted that an RAPD is not caused by either cataract or vitreous haemorrhage, and when associated with amblyopia is at most a mild RAPD. A Definite RAPD in these cases should prompt a look for another cause of visual loss.

How to Examine Normal Pupils

2009-03-06T04:44:00.000-08:00

Hi

A normal pupil examination can be documented as being PERL and NO RAPD. This shorthand states that the pupils are equal and reactive to light, and that there is no Relative Afferent Pupil Defect.

So how do I actually test these properly?

I ask to patient to fix in the distance, then i check the pupils are equal in size, and again with the lights off. Then, with the lights still off I check each eye has a direct response to light. Finally I do a swinging light test to check there is no RAPD.

Now lets recap with a little more explanation.

Firstly To avoid the near reflex where the eyes converge, accommodate and the pupils constrict, ask the patient to fix on an object in the distance.

You should check the pupils are equal in both light and dark or you may miss an abnormally small pupil such as is seen in horner's syndrome. For more on unequal pupils watch the video titled anisocoria.

When examining the pupil reactions, having the patient in the dark with distance fixation makes the pupils as large as possible and makes the pupil reactions easier to see.

When you shine the light at the pupil, watch the same pupil for a quick constriction, followed by a slight relaxation.

There is no need to look for a consensual reaction here as both eyes have demonstrated a direct reaction indicating an intact afferent pathway from eye to brain, and efferent pathway from brain to pupil. There is also no need to check for a response to accommodation unless the pupils fail to respond to light.

Finally the swinging light test to check for a relative afferent pupil defect or RAPD. This is a comparative test of the two optic nerves, and may detect conditions such as optic neuritis or optic nerve compression where the nerve is functioning, but poorly when compared to the other side.
Again this should be in the dark with distance fixation. First shine the light at the first eye, the pupil will constrict and then relax a little, now swing the light source, quickly and directly, to the other eye. The pupil will have just started to dilate when the light hits it, causing a small constriction, followed by a relaxation. Make sure you hold the light on each eye for 2 to 3 seconds to allow each pupil to first constrict then relax before you swing the light to the other eye.

Your light source must be bright to reliably detect an RAPD, a standard direct ophthalmoscope or pen torch may not be bright enough.

OK, you have now examined these normal pupils.

ooops

2009-02-03T03:17:00.000-08:00

having pressed the wrong button, i have deleted this blog.
I will put the transcripts back up soon!

The video's are still all at youtube.com/stapsell