8.1.7 Manages pxs presenting with an incomitant deviation Flashcards
What is an incomitant deviation?
Angle of deviation varies in different directions of gaze. Can be mechanical or neurological.
The development of comitance in long standing cases results in equality in the size of
primary and secondary deviations
o BSV may be maintained by the use of CHP or increased fusional amplitude
o Acquired - Acute onset results in diplopia - Incomitant
o Congenital – may result in suppression or CHP – Concomitant
What are the steps to muscle sequelae and how long do they take to develop?
- Determined by Hering’s Law of equal innervation and Sherrington’s Law of reciprocal innervation
o Step 1 – Primary Palsy (Under action) – e.g. UA of Right SR (Palsy) - immediate
o Step 2 – Over Action of Contralateral Synergist – e.g. OA of Left IO - immediate
o Step 3 – Over Action of the ipsilateral Antagonist – e.g. OA of Right IR - week or 2 to a few weeks
o Step 4 – Secondary inhibition palsy of the contralateral antagonist – e.g. UA of Left SO - takes more time
What are the signs of a neurological deviation?
Definition: Lack of innervation to an eye muscle (due to nerve transmission issues)
Deviation: Large
Movement: Slowly stops
Diplopia: in the direction of the affected muscle
Globe Retraction: Absent
Pain: Absent
Management: Emergency as cause is usually a compressive lesion/vascular
What are the signs of a mechanical deviation?
Definition: Factors within the orbit which interfere with muscle contraction & relaxation or otherwise
prevent free movement
Deviation: Small
Movement: Abruptly stops
Diplopia: in the opposite direction of the affected muscle
Globe Retraction: Present
Pain: Usually Present
Management: Routine if congenital, otherwise urgent
What should you look for in an incomitant deviation?
- Diplopia
- Head posture to avoid dip
- A/V pattern
Describe a 3rd cranial nerve palsy?
o Anatomy – Originate in the pons at the oculomotor nucleus passes through the circle of willis (runs
parallel to the Posterior communicating artery(PCA)) through the cavernous sinus and splits in the
superior and inferior divisions.
o Anatomy – Innervates the medial rectus (MR), Inferior rectus (IR), Superior rectus (SR), inferior oblique (IO),
Ciliary body, Iris Sphincter
o Causes – Posterior communicating artery aneurysm, pressure from space occupying lesion, microvascular disease
EMERGENCY REFERRAL
Sudden Onset
* Unilateral
* Ptosis
* Diplopia
* H/A
* Pupil Dilation
What is a total 3rd nerve palsy?
▪ Exotropic, hypotropic and intorted eye with/without dilated pupil, cycloplegia
and ptosis (Complete Palsy)
▪ Limited adduction, limited elevation, limited depression, normal abduction
what is a superior division 3rd NP?
▪ Congenital most common if acquired then usually aneurysm
▪ Superior Rectus and Levator affected
▪ Eye Hypotropic with ptosis
▪ Muscle sequelae – O/A of contralateral IO, contracture of ipsilateral IR,
secondary inhibition palsy of contralateral SO
▪ CHP – chin up, face turn to unaffected side
What is an inferior division 3rd NP?
▪ Medial rectus, Inferior rectus and inferior oblique, sphincter pupillae and
ciliary muscle affected
▪ Eye Exotropic, intorted, Hypertropic
▪ Sequelae – O/A of contralateral LR, SR, and SO
▪ Accommodation affected
Describe pupil involvement in 3rd NP?
▪ 3rd cranial nerve runs parallel to the PCA
▪ Blood vessels on pia mater supply surface of the nerve INCLUDING pupillary
fibres so a compressive lesion (aneurysms on PCA) will cause PUPIL DILATION.
▪ Vaso Vasorum supplies part of the nerve but NOT the pupillary fibres and is
more prone to damage by conditions such as diabetes and thus DOES NOT cause
pupil dilation.
Describe a 4th cranial nerve palsy?
o Anatomy – Originates in the nucleus in the midbrain at the level of the inferior colliculus and proceed
posteriorly and crossover before making their way to the eye (longest and thinnest nerve) passes through
the circle of willis
o Anatomy – Innervates the superior oblique (SO), longest thinnest nerve, easily damaged in soft head or body
trauma
o Congenital or Acquired – Bilateral unless proven otherwise
o closed head injury, diabetes, space occupying lesion and myasthenia gravis
* Sudden Onset,
* Vertical Diplopia,
* Hypertropia
Describe a unilateral 4th CN palsy?
usually congenital
▪ Affects SO
▪ Eye Hypertropic and Esotropic
▪ May control hypertropia with CHP – chin depression, face turn to affected eye,
head tilt to unaffected (lower) eye
▪ Adaptation to torsion
Describe a bilateral 4th CN palsy?
▪ V eso pattern
▪ Significant extorsion >10 degrees therefore torsional diplopia the greatest
symptom
▪ CHP - chin depression
▪ +ve BHTT to either side
▪ Reversal of hypertropia on dextrodepression and laevodepression
What is the Bielschowsky Head Tilt Test (BHHT)?
Tilt head to either side and assess
vertical deviation. Greater when tilted to affected side if SO palsy due to
intorsional and elevating action of ipsilateral SR.
Describe a 6th cranial nerve palsy?
o Anatomy – Originates in the nucleus in the pons ventral to the floor of the
fourth ventricle -> moves vertically and a 90-degree bend over the petroclinoid
ligament -> petrous temporal bone -> Dorello’s canal -> cavernous sinus -> superior orbital fissue -> to the LR
o Anatomy – Innervates the Lateral Rectus (LR) prone to damage due to raised intra-cranial pressure
o Acquired
o Nerve Nucleus – Demyelination, vascular, space occupying lesion
o Long intracranial course – compression as the nerves passes over petrous
temporal bone due to raised ICP, aneurysms, space occupying lesion
o Features – Esotropia greatest on distance fixation
o CHP – face turn to affected side
o Sequelae – O/A of contralateral MR, O/A of ipsilateral MR, U/A of
contralateral LR
o Unilateral or Bilateral
o Esotropia (eye turns in)
* Sudden Onset
* Horizontal Diplopia
IN CHILDREN: who have esotropia, optic disc swelling and headaches which are worse in morning they may have 6th CNP due to raised intracranial hypertension - get px to turn head to L and R and do cover test - if eso is bigger to one side then there is LR underaction = EMERGENCY REFERRAL
Describe myasthenia gravis?
- Autoimmune disorder – causes excessive fatigability of striated muscles
o Signs & Symptoms – Ocular fatigue, systemic fatigue, diurnal variation as the day progresses, weakness
increases after exercise, common in younger females and older males.
o Ocular –
▪ Ptosis – often the initial sign, bilateral and asymmetrical, frontalis over-action is often seen in
attempt to elevate eye, elevate eyelids for 1-2 mins ptosis worse on return to primary position,
Cogan lid twitch – px depresses for 15 secs on return to primary position lid initially elevate above
ptotic level before returning to normal position. Gorelicks sign – in asymmetrical cases hold the
more ptotic lid and the ptosis on the opposite side will increase.
▪ Diplopia – Variable may change horizontal to vertical, px may report that images separate further as
fatigue increases, may mimic palsies and change which muscle is affected.
▪ Orbicularis weakness – can close eyes but unable to stop examiner opening eyes with gentle
pressure
▪ Treatment – Ptosis props, Occlusion, Surgery is contraindicated due to instability. Immunosuppression with steroid - 10mg prednisolone. - If systemic MG then phone GP & say concerned about px
- If ocular MG ONLY then refer patient urgently
- SYSTEMIC SXS: chewing and speech difficulties, breathlessness, fatigue, lack of facial expressions
Describe thyroid eye disease and Graves Ophthalmopathy?
- Eye disease associated with over action of thyroid gland (hyperthyroidism) is called thyrotoxicosis. Eye disease
associated with under action of thyroid gland (hypothyroidism) is called myxodema - Symptoms
o Discomfort – drying of corneal epithelium, proptosis, lid retraction, swollen conjunctiva
o Loss of VA – Cornea exposure, optic nerve compression
o Diplopia – vertical/horizontal due to oedema and EOM fibrosis - Signs
o Lid Retraction (over action of muller muscle, Lid lag on down gaze, Proptosis,
Oedema, Motility Disorder – IR most commonly affected then MR, esotropia and
hypotropia most common, CHP to increase field of BSV, conjunctival Chemosis,
corneal erosion, increase in IOP on elevation - Graves Ophthalmopathy – this condition refers to the inflammatory response
and its sequelae in and around the orbit associated with autoimmune thyroid
disease. most often associated with hyperthyroidism but does occur with
hypothyroidism.
o Active (WET) Phase – EOM (extra-ocular muscles) become swollen due to
infiltration by lymphocytes, oedema cause EOM enlargement by 10%. This
causes proptosis, corneal exposure and VF loss due to ON compression, Lid
retraction.
o Restrictive Myopathy – due to fibrotic contracture of EOM (restriction in
elevation most common then ABDuction, depression and ADDuction) IR-> MR->SR->LR
o Inactive (DRY) Phase – fibrosis and secondary EOM contracture, muscle bulk
reduces so proptosis reduces, EOM restriction stabilises, enlarged vertical fusion
range, diplopia and lid retraction.
o Active Treatment – Systemic steroids, surgical decompression, radio therapy, corneal lubricants
o Inactive Treatment – Lateral tarsorrhaphy, BT or prism therapy, surgery to increase BSV, lid retraction
surgery
Describe Duane’s syndrome?
- Type I:
o Marked limitation of abduction & widening of palpebral fissure due to lack of innervation to LR
o Normal or slight limitation of adduction w/ narrowing of palpebral fissure & retraction of globe due to maximum innervation of LR when eye is adducted (due to co-contraction of MR & LR)
o THINK TYPE 1 ONLY HAS ONE ‘d’ – eye will be more eso - Type II:
o Limitation of adduction by co-contraction of horizontal recti on attempted adduction with normal or slightly reduced abduction
o THINK TYPE 2 HAS 2 ‘ds’ – eye will be more exo - Type III:
o Limitation of both adduction & abduction
o EYE WILL HAVE BOTH ESO & EXO – most common type
o Characteristic
▪ Poor Convergence
▪ CHP – face turn to affected side (except Type C), A or V Patterns
▪ Up shoots and Down shoots on ADDuction
o Associated Developmental Defects
▪ Coloboma, Heterochromia, Len Opacities, Ear Malformation, Cleft Palate
o Management -
▪ If BSV good and cosmetically acceptable CHP then observe only
▪ If CHP causing neck problems or poor cosmesis – surgery to enhance abduction ability
▪ If manifest in primary position then prism and surgery – Recession procedures
Refer to HES if 1st presentation
Describe Brown’s syndrome?
Limited elevation of the eye on ADDuction with normal depression in
ADDuction
oCharacteristics –
▪ Unilateral, most px have BSV but some has strabismus in primary
position
▪ Limitation of elevation in ADDuction and direct elevation
▪ Down drift of affected eye on contralateral version, Over action of
contralateral superior rectus
▪ A or V Pattern, CHP head tilt to affected eye or chin elevation in
bilateral Brown’s
* Causes –
o Short superior oblique anterior tendon sheath, Short superior oblique tendon, can be caused by
inflammation or trauma to trochlear region, Nodule or swelling on the superior oblique
* Treatment –
o Non-surgical – If BSV present and deviation well compensated observe and monitor BSV. Treat any underlying inflammatory conditions
o Surgical – Explore tendon, sheath and trochlear region, possible recession contralateral superior rectus,
possible steroid injection if nodule present
If 1st presentation then refer to HES
